<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.bloodreviews.com/?rss=yes"><title>Blood Reviews</title><description>Blood Reviews RSS feed: Current Issue.    
 
 
 
This respected international journal,  Blood Reviews , is a vital information resource, bringing 
together appraisals of clinical practice, and research from recognized experts. Specially commissioned articles from leading researchers 
and practitioners guarantee truly global coverage of all the sub-specialties of hematology. 
 
 Blood Reviews  publishes review 
articles covering the spectrum of clinical and laboratory haematological practice and research. Although most reviews are invited, the 
editors welcome suggestions from potential authors. They should first write a brief outline of an intended review and send this to Dr 
Trevor Baglin or to Dr Jacob M Rowe. 
   </description><link>http://www.bloodreviews.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2011 Elsevier Ltd. All rights reserved. </dc:rights><prism:publicationName>Blood Reviews</prism:publicationName><prism:issn>0268-960X</prism:issn><prism:volume>26</prism:volume><prism:number>2</prism:number><prism:publicationDate>March 2012</prism:publicationDate><prism:copyright> © 2011 Elsevier Ltd. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.bloodreviews.com/article/PIIS0268960X11000701/abstract?rss=yes"/><rdf:li rdf:resource="http://www.bloodreviews.com/article/PIIS0268960X11000804/abstract?rss=yes"/><rdf:li rdf:resource="http://www.bloodreviews.com/article/PIIS0268960X11000816/abstract?rss=yes"/><rdf:li rdf:resource="http://www.bloodreviews.com/article/PIIS0268960X11000828/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.bloodreviews.com/article/PIIS0268960X11000701/abstract?rss=yes"><title>Apoptosis in the anucleate platelet</title><link>http://www.bloodreviews.com/article/PIIS0268960X11000701/abstract?rss=yes</link><description>Abstract: For many years, programmed cell death, known as apoptosis, was attributed exclusively to nucleated cells. Currently, however, apoptosis is also well-documented in anucleate platelets. This review describes extrinsic and intrinsic pathways of apoptosis in nucleated cells and in platelets, platelet apoptosis induced by multiple chemical stimuli and shear stresses, markers of platelet apoptosis, mitochodrial control of platelet apoptosis, and apoptosis mediated by platelet surface receptors PAR-1, GPIIbIIIa and GPIbα. In addition, this review presents data on platelet apoptosis provoked by aging of platelets in vitro during platelet storage, platelet apoptosis in pathological settings in humans and animal models, and inhibition of platelet apoptosis by cyclosporin A, intravenous immunoglobulin and GPIIbIIIa antagonist drugs.</description><dc:title>Apoptosis in the anucleate platelet</dc:title><dc:creator>Valery Leytin</dc:creator><dc:identifier>10.1016/j.blre.2011.10.002</dc:identifier><dc:source>Blood Reviews 26, 2 (2012)</dc:source><dc:date>2011-11-07</dc:date><prism:publicationName>Blood Reviews</prism:publicationName><prism:publicationDate>2011-11-07</prism:publicationDate><prism:volume>26</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0268-960X(12)X0002-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>51</prism:startingPage><prism:endingPage>63</prism:endingPage></item><item rdf:about="http://www.bloodreviews.com/article/PIIS0268960X11000804/abstract?rss=yes"><title>The investigation and treatment of secondary anaemia</title><link>http://www.bloodreviews.com/article/PIIS0268960X11000804/abstract?rss=yes</link><description>Abstract: Secondary anaemia or the anaemia of chronic disease (ACD) is the commonest form of anaemia in hospitalised patients and the second most prevalent anaemia worldwide after iron deficiency. It is characterised by defective iron incorporation in erythropoiesis, an impaired response to erythropoietin, a decrease in erythropoietin production and cytokine induced shortening of red cell survival.For many patients with ACD the cause is apparent but for many others the underlying disease needs to be determined and such patients are often referred to haematologists for investigation. The search for the cause can be a fascinating exercise in good history taking, examination skills and performing and interpreting appropriate investigations. This review covers the pathogenesis and causes of ACD and then discusses the clinical and laboratory investigation of a patient with suspected ACD. Finally, the management of a patient with ACD is discussed including erythropoiesis stimulating agents (ESAs), intravenous iron and future therapies.</description><dc:title>The investigation and treatment of secondary anaemia</dc:title><dc:creator>Sarah L. Davis, T.J. Littlewood</dc:creator><dc:identifier>10.1016/j.blre.2011.10.003</dc:identifier><dc:source>Blood Reviews 26, 2 (2012)</dc:source><dc:date>2011-12-02</dc:date><prism:publicationName>Blood Reviews</prism:publicationName><prism:publicationDate>2011-12-02</prism:publicationDate><prism:volume>26</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0268-960X(12)X0002-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>65</prism:startingPage><prism:endingPage>71</prism:endingPage></item><item rdf:about="http://www.bloodreviews.com/article/PIIS0268960X11000816/abstract?rss=yes"><title>MDS: Refining existing therapy through improved biologic insights</title><link>http://www.bloodreviews.com/article/PIIS0268960X11000816/abstract?rss=yes</link><description>Abstract: Advances in therapy can essentially be measured using two parameters; introduction of a new agent which benefits an increased number of patients over prevailing treatments or more selective use of an existing drug by matching it to the biologic characteristics associated with response. In reviewing the therapeutic landscape of myelodysplastic syndromes (MDS), both should be applied to gauge the advances in therapy. While several new drugs are currently in clinical trials for the treatment of MDS, three drugs were approved for use in the last decade and sufficient time has elapsed to take stock of the benefit they have produced in the outcome of patients both in terms of survival and quality of life. For the two hypomethylating agents, response remains limited to 50% patients at best, and no strategy has evolved to allow for pre-selection of likely responders, however, 5-azacytidine has been associated with improvement in the survival of higher risk patients. The benefit of lenalidomide was found to be greater for del(5q) patients with transfusion dependent anemia and lower risk disease right from the start, although a quarter of the non-del(5q) patients also experienced complete transfusion independence with this agent. It is in this latter group of non-del(5q) cases that a strategy for potentially preselecting likely responders is suggested by the finding of an expression profile associated with response. In this paper, we will focus on defining our current understanding of the mechanisms of action of the existing FDA approved drugs in order to identify therapeutic strategies that are suitable for specific MDS subtypes. We expect that through advancing biologic insights, the use of such therapies will become more selective and refined.</description><dc:title>MDS: Refining existing therapy through improved biologic insights</dc:title><dc:creator>Jordan Schecter, Naomi Galili, Azra Raza</dc:creator><dc:identifier>10.1016/j.blre.2011.11.001</dc:identifier><dc:source>Blood Reviews 26, 2 (2012)</dc:source><dc:date>2011-12-02</dc:date><prism:publicationName>Blood Reviews</prism:publicationName><prism:publicationDate>2011-12-02</prism:publicationDate><prism:volume>26</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0268-960X(12)X0002-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>73</prism:startingPage><prism:endingPage>80</prism:endingPage></item><item rdf:about="http://www.bloodreviews.com/article/PIIS0268960X11000828/abstract?rss=yes"><title>Ex-vivo expansion of red blood cells: How real for transfusion in humans?</title><link>http://www.bloodreviews.com/article/PIIS0268960X11000828/abstract?rss=yes</link><description>Abstract: Blood transfusion is indispensable for modern medicine. In developed countries, the blood supply is adequate and safe but blood for alloimmunized patients is often unavailable. Concerns are increasing that donations may become inadequate in the future as the population ages prompting a search for alternative transfusion products. Improvements in culture conditions and proof-of-principle studies in animal models have suggested that ex-vivo expanded red cells may represent such a product. Compared to other cell therapies transfusion poses the unique challenge of requiring great cell doses (2.5×1012 cells vs 107 cells). Although production of such cell numbers is theoretically possible, current technologies generate red cells in numbers sufficient only for safety studies. It is conceived that by the time these studies will be completed, technical barriers to mass cell production will have been eliminated making transfusion with ex-vivo generated red cells a reality.</description><dc:title>Ex-vivo expansion of red blood cells: How real for transfusion in humans?</dc:title><dc:creator>Anna Rita Migliaccio, Elena Masselli, Lilian Varricchio, Carolyn Whitsett</dc:creator><dc:identifier>10.1016/j.blre.2011.11.002</dc:identifier><dc:source>Blood Reviews 26, 2 (2012)</dc:source><dc:date>2011-12-19</dc:date><prism:publicationName>Blood Reviews</prism:publicationName><prism:publicationDate>2011-12-19</prism:publicationDate><prism:volume>26</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0268-960X(12)X0002-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>81</prism:startingPage><prism:endingPage>95</prism:endingPage></item></rdf:RDF>
